IGA NEPHROPATHY (IGAN) OCCURS WHEN THE BODY GENERATES ABNORMAL VERSIONS OF IGA.

IgA is an antibody that is part of the immune system and when IgAN occurs, abnormal versions of IgA that are deficient in the sugar galactose (referred to as Gd-IgA1) are generated. The immune system misrecognizes Gd-IgA1 as a foreign antigen and generates auto-antibodies that bind to the Gd-IgA1, forming immune complexes, which are large pathogenic molecules that circulate through the blood and deposit in the kidney. The deposits of the immune complexes cause kidney inflammation and kidney damage.

There is no prevention or cure of IgAN. Current medical standard-of-care can cause unwanted side effects and may broadly and non-specifically suppress the patient’s immune systems, resulting in increased risk of infections and other complications.

HOW SIBEPRENLIMAB CAN HELP

Sibeprenlimab reduces the production of Gd-IgA1 by binding to a specific signaling molecule called APRIL (short for “A Proliferation-Inducing Ligand”), which is believed to be a driver of IgA and Gd-IgA1 production. By binding and neutralizing APRIL, Sibeprenlimab may reduce the amount of IgA and Gd-IgA1. Lower levels of Gd-IgA1 may then result in reduced auto-antibody production, which in turn may result in fewer immune complexes, decreased immune complex deposits in kidney, and reduced kidney inflammation. By reducing the production of Gd-IgA1, Sibeprenlimab is believed to prevent further kidney damage and the progression to end stage kidney disease.